Local Inflammatory Markers and Systemic Endotoxin in Aggressive Periodontitis
Local Inflammatory Markers and Systemic Endotoxin in Aggressive Periodontitis
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DOI：
10.1177/0022034511413928
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发表时间：
2011-09-01
影响因子：
7.6
通讯作者：
Wallet, S. M.
中科院分区：
文献类型：
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作者：
Shaddox, L. M.;Wiedey, J.;Wallet, S. M.
虽然许多研究都集中在局部和全身因素导致牙周病，很少有人知道有关这些因素的机制。我们以前曾报道过局部侵袭性牙周炎（牙周炎）对细菌内毒素的全身性炎症反应。本研究的目的是描述龈沟液（GCF）中的细胞/趋化因子，并评估与牙龈炎相关的全身内毒素水平。临床参数、GCF和外周血收集自：34名患者、10名健康同胞和9名健康无关对照个体。定量GCF中的细胞因子/趋化因子，定量血浆中的全身内毒素水平，并在所有参数之间进行相关性分析。与健康部位相比，9种介质在子宫内膜病变部位升高（TNF α、INF γ、IL 1 β、IL 2、IL 6、IL 10、I112 p40、GMCSF和MIP 1 α，p < 0.001），而MCP 1、IL 4和IL 8在健康部位升高（p < 0.01）。与健康受试者相比，在受试者血浆中检测到高出4至5倍的内毒素水平（p < 0.0001），这与所有临床参数和分析的大多数细胞/趋化因子相关。总之，在EAE中发现了更高的全身内毒素水平，这与局部炎症反应加剧和疾病的临床体征相关。（Clinicaltrials.gov编号，NCT 01330719）。
While much research has focused on local and systemic factors contributing to periodontal disease, little is known regarding mechanisms linking these factors. We have previously reported a systemic hyper-inflammatory response to bacterial endotoxin in localized aggressive periodontitis (LAP). The objectives of this study were to delineate cyto/chemokines in gingival crevicular fluid (GCF) and evaluate systemic levels of endotoxin associated with LAP. Clinical parameters, GCF, and peripheral blood were collected from: 34 LAP, 10 healthy siblings, and nine healthy unrelated control individuals. Cyto/chemokines were quantified in GCF, systemic endotoxin levels were quantified in plasma, and correlation analysis was performed among all parameters. Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNF alpha, INF gamma, IL1 beta, IL2, IL6, IL10, I112p40, GMCSF, and MIP1 alpha, p < 0.001), while MCP1, IL4, and IL8 were elevated in healthy sites (p < 0.01). Four- to five-fold-higher endotoxin levels were detected in LAP plasma compared with that from healthy participants (p < 0.0001), which correlated with all clinical parameters and most cyto/chemokines analyzed. In conclusion, higher systemic levels of endotoxin were found in LAP, which correlates with an exacerbated local inflammatory response and clinical signs of disease. (Clinicaltrials.gov number, NCT01330719).